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Platelet-rich plasma inhibits inflammation, apoptosis, and the NLRP3/Caspase-1 pathway and induces matrix metalloproteinases and proliferation of IL-1β-induced articular chondrocytes by downregulating T-box transcription factor 3

基质金属蛋白酶 细胞凋亡 MMP9公司 炎症 污渍 富血小板血浆 软骨细胞 化学 下调和上调 癌症研究 细胞生物学 分子生物学 免疫学 体外 医学 生物 血小板 生物化学 基因
作者
Zhuo Feng,Jun Li,Yonghong Wang,Ming Li,Frank M. Song,Yuliang Liu,Zong-Yu Tao
出处
期刊:European Journal of Inflammation [SAGE]
卷期号:20: 1721727X2210930-1721727X2210930 被引量:2
标识
DOI:10.1177/1721727x221093056
摘要

Objectives Osteoarthritis (OA) is a chronic joint disease characterized by osteoproliferation and the degeneration and destruction of articular cartilage. Platelet-rich plasma (PRP) is rich in various growth factors that have been reported to promote bone defect repair. This study examined the specific role and mechanism of PRP in OA. Methods OA model cells were created by treating articular chondrocytes with IL-1β. After treatment of the model cells with PRP or/and a T-box transcription factor 3 (TBX3)-overexpression plasmid, TBX3 expression was monitored via RT-qPCR, western blotting, and immunofluorescence assays. IL-1β, IL-33, and Caspase-3 levels were detected with ELISA kits. Levels of NLRP3, Caspase-1, MMP9, MMP13, and COL2A1 expression were evaluated by western blotting, and cell proliferation was assessed by the CCK-8 assay. Results Our results showed that TBX3 expression was upregulated in IL-1β-induced articular chondrocytes. IL-1β stimulation induced inflammation and the production of matrix metalloproteinases, activated Caspase-3 and the NLRP3/Caspase-1 pathway, inhibited the proliferation of articular chondrocytes; however, all those affects mediated by IL-1β could be markedly reversed by PRP. We also found that PRP alleviated IL-1β-induced inflammation, apoptosis, and extracellular matrix degradation in articular chondrocytes by inhibiting TBX3. Our findings suggest that PRP alleviates OA progression in vitro by downregulating TBX3. Conclusion PRP suppressed OA progression in vitro by inhibiting TBX3, which may be its mechanism of action in treating OA.
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